INTRODUCTION

Many forms of nonischemic cardiomyopathy (NICM) are associated with prominent epicardial scarring, which frequently surpasses the amount of scar at the endocardial counterpart. Consequently, a significant number of NICM-related ventricular tachycardia (VT) circuits and exit sites are located at the epicardial and subepicardial layers of the right (RV) and left ventricle (LV).^1–4 This is in contrast to the usual scar distribution pattern in ischemic cardiomyopathies (ICM), in which endocardial/subendocardial scarring and VT origins are manifestly predominant.^1,2

Up to 90% of LV VTs in NICM patients originate from substrate-based abnormalities located near the lateral perivalvular aortic and (especially) mitral valve regions, with epicardial involvement in most cases, corresponding with the so-called (infero-) lateral NICM scar distribution pattern.^5,6 The alternative anteroseptal pattern accounts for the remaining NICM LV VTs, which predominantly arise from intraseptal VT circuits.⁶

Epicardial VTs in the setting of RV cardiomyopathy usually originate from the free-wall basal inferior RV and from the infundibular anterior portion of the RV, close to the interventricular groove but not reaching the RV septum (low right ventricular outflow tract, in particular the subpulmonary infundibulum).^4,7 The third RV area of frequent histological abnormality, the RV apex, is not a frequent exit site of origin of RV cardiomyopathy-related VTs. From the very initial surgical experiences until the most recent catheter ablation series, it is demonstrated that the typical histological pattern of muscular replacement by fatty or fibrofatty tissue, with strands of myocardium responsible for myocardial reentry embedded, is predominantly epicardial or subepicardial, thus setting up the potential for failure to eliminate VT from the endocardium.^4,7–11 Epicardial VTs are the rule in RV cardiomyopathy, although some of them are still amenable to successful ablation from the endocardial surface. This especially accounts for advanced stages of the disease, in which there is a shift toward a more prominent endocardial VT substrate due to dense and compact scarring at the epicardial surface.¹²

To identify a probable epicardial exit site of the VT (an area frequently targeted for ablation) prior to the VT ablation procedure is of high interest: a probable need to gain access to the epicardium needs to be specifically discussed with the patient, due to the particular risks inherent to the percutaneous epicardial intervention. In this scenario, a thorough analysis of the 12-lead VT QRS complex helps to identify a probable epicardial exit of the ventricular arrhythmia, a frequent scenario in the setting of NICM VT.

The initial few milliseconds within the VT-QRS complex are the result of the ventricular wall’s transmural depolarization, from the epicardium toward the endocardium in epicardial VTs and in the opposite direction during free-wall endocardial VTs.¹³ Most of the 12-lead electrocardiogram (ECG) signatures indicating an epicardial VT origin are based on the interval measurement and morphological characterization of the VT-QRS initial portion.

In this chapter, a guide for using the 12-lead ECG in order to identify an epicardial VT exit site in the setting of NICM is provided.

ECG CRITERIA SUGGESTING AN EPICARDIAL VT ORIGIN IN LV NONISCHEMIC CARDIOMYOPATHY

The vast majority of LV VTs in the setting of NICM arise from the epicardial aspect of the basal-lateral LV free wall. In this setting, the transmural ventricular activation slowly propagates from the epicardial/subepicardial layers toward the endocardium until it engages the subendocardial specialized Purkinje network, rapidly depolarizing both ventricles thereafter. Such slow (cell-by-cell) initial depolarization mimics the delta wave that is characteristic of the preexcitation syndromes (Figure 20.1). The interval criteria identifying an epicardial VT site of origin are based on the recognition and measurement of this initial slurred portion of the QRS complex (Figure 20.2).^14–16 Interestingly, the vast majority of patients from whom these interval criteria were developed had underlying ICM or no underlying structural heart disease, thus raising the concern about their applicability to a NICM setting.¹⁷

Figure 20.1 Rationale for initial QRS slurring during epicardial ventricular tachycardia. In this histological view of the left ventricular free wall, the subendocardial disposition of the Purkinje network is depicted and the simulated initial vectors of ventricular depolarization during endocardial and epicardial VT are drawn (arrows). Please note, engagement of the specialized conducting system occurs faster during endocardial VT than during epicardial VT, the latter thus registering a manifest initial slurring of the VT QRS complex (mimicking the delta wave observed in WPW patients), in which interval criteria are based on. Abbreviations: Endo, endocardium; Epi, epicardium; VT, ventricular tachycardia.

Importantly, the total VT-QRS complex duration repeatedly proved useless to differentiate epicardial from endocardial VTs, due to significant overlap in QRS width between epicardial and endocardial VTs, although a value of > 211 ms has been suggested as fairly specific to epicardial VTs.15,17,18

Since none of the defined interval criteria had been primarily developed in the specific setting of patients with right or left NICM, with the basal lateral LV region also being underrepresented, additional work was required to adapt such interval criteria to basal superior and lateral NICM LV VTs, clearly the most frequent VT site of origin in this setting.¹⁹ The revisited cutoff values for the pseudodelta wave, the intrinsicoid deflection time, the shortest RS complex, and the maximum deflection index, however, yielded lower sensitivity and specificity values than initially described. The diagnostic accuracy of the interval criteria was further noted to be region-dependent, with a significant variability of the sensitivity and specificity values between basal, mid-wall, or apical and inferior, lateral, or anterior LV locations.

It can be summarized that the recognition of an initial VT-QRS slurring in the setting of NICM should raise the suspicion of an epicardial origin. The proposed interval criteria should be applied with caution in this setting: the NICM nature of the cardiomyopathy and its variable transmural scar distribution pattern, the LV region of interest, the degree of the LV remodeling/dilatation, the local wall thickness within the VT region of origin, and the presence/absence of baseline conduction system disturbance may dramatically influence the value of the pseudodelta wave and other interval criteria in the setting of NICM (Figure 20.3).^17,20

The bundle branch pattern in lead V1, the QRS width and axis, the QRS concordance in the precordial leads and its polarity in leads V3 and V4 are useful ECG tools that help to regionalize the VT site of origin.21–23

Stay updated, free articles. Join our Telegram channel

Join